The present invention generally relates to a disease treatment method, and more specifically to a method for treating malaria.
Malaria is a dangerous disease caused by a protozoic parasite which invades a host's liver cells and erythrocytes. It is one of the most wide-spread infectious diseases. The World Health Organization estimates that 200,000,000 people are infected with the malaria parasite annually. These people mainly reside in the tropics. One million cases of malaria were reported in the U.S. in 1940. At that time, effective measures were introduced which virtually eliminated the disease, which is transmitted by the female Anopheles mosquito. However, the Anopheles mosquito is still present in many of the Southern and Western parts of the U.S. During the early 1970's, there were several cases of malaria reported in Louisiana and California. These were attributed to returning veterans from the Viet Nam War who harbored the parasite.
As tropical regions of the world become more accessible through improved modes of transportation, travel into these areas is increasing. This has resulted in significantly more cases of malaria being reported in travelers returning from these areas. One percent (1%) of all people infected with the malaria parasite die from the disease (2,000,000 people per year). There are four species of Plasmodium which infect humans and cause malaria. These include P. falciparum. P. vivax, P. ovale, and P. malariae. P. falciparum is the most serious species. It is responsible for cerebral malaria which is associated with a 50% mortality rate.
The life cycle of a Plasmodium parasite involves the interrelationship between an Anopheles mosquito vector and a mammalian host. When an uninfected female Anopheles mosquito bites and ingests blood from a host harboring the sexual forms of the Plasmodium parasite, the parasitic life cycle begins. In the Anopheles, the male and female gametocytes fuse and travel after several stages of development to the salivary glands of the mosquito. The parasite at this stage is called a "sporozoite." If the infected mosquito bites a new host, the sporozoites are injected into the host's blood. Thereafter, they travel to the liver within 30 minutes, where they enter a liver cell. In the liver cell, one sporozoite multiplies and forms about 10,000-20,000 merozoites. These merozoites are released from the liver cells in 10-12 days. Each of the released merozoites immediately invades an erythrocyte. In 48 hours, each merozoite forms another 10-12 merozoites which are in turn released from the erythrocyte only to invade another 10-12 erythrocytes.
The clinical manifestations of the disease include fever, headaches, sweating, vomiting, and prostration. These manifestations occur simultaneously with merozoite release from the erythrocytes. The erythrocyte reinvasion occurs until the host dies, or until the host's immune system is able to control and suppress merozoite activity. At some point, the merozoites (previously asexual) differentiate into male and female gametocytes. The technical and scientific basis for this transformation is an active area of current medical research. If a female Anopheles then bites a new host at the time of gametocyte formation, the life cycle of the parasite is completed.
The most susceptible human hosts for the disease are infants and pregnant women having suppressed immunity. Recently, deaths have been reported in adult male AIDS patients caused by cerebral malaria. In addition, non-immune travelers into high-risk malaria areas are also susceptible to the disease, especially with respect to chloroquine and quinine resistant malaria.
There is a natural immunity to malaria which develops in persons living in high-risk malaria areas. This immunity appears to depend upon the continual presence of low parasite levels in the host's body. This conclusion is drawn from many studies which demonstrate that when persons living in high-risk malaria areas leave for a variety of reasons and travel to low risk areas, they substantially lose their immunity.
Many chemical agents have been developed to treat malaria. For example, chloroquine and quinine have been used over the past thirty years. However, chloroquine-resistant malaria strains of P. falciparum (the malaria parasite responsible for 1.6 million deaths annually) have spread from two to seventy countries throughout the world. In addition, there are twelve countries which have reported quinine-resistant strains of P. falciparum. As a result, many corporations and governments have spent billions of dollars in attempts to develop new drug therapies for the disease, with an inconsequential degree of success.
The present invention represents a new and effective therapeutic method for treating malaria. It offers a superior degree of efficacy, safety, and utility compared with currentlyused compounds.